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COPS5 activates cell population proliferation. 47 / 57
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"Also, Jab1 activate the c-jun gene resulted cell proliferation."
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"Overexpression of JAB1 promoted the proliferation, migration, and invasion of ESCC cells, and was significantly associated with poor prognosis of ESCC patients."
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"In line with this finding, knockdown of CSN5 and CSN4 in cultured cells can significantly reduce the rate of cellular proliferation; this proliferation defect can be fully rescued by forced expression[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"
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"Our data demonstrated that Jab1 protein was a vital upstream negative modulation factor of p14ARF, and Jab1 could promote cell proliferation and tumor growth via inhibiting the expression of p14ARF in vivo and in vitro."
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"Our previous studies showed that Jab1 and COPS5 was highly expressed in breast cancer and played an essential role in the breast cancer pathogenesis, and that Jab1 knockdown significantly inhibited breast cancer cell proliferation and metastasis."
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"Taken together, our results suggest that Trx may regulate cell cycle and growth through a novel modulation of Jab1 mediated proliferation signals, further indicating that Trx may have the ability to control tumor progression."
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"In addition, Hsieh et al. demonstrated that the pre-S2 LHBS mutant induces the Ub-dependent proteasomal degradation of cyclin-dependent kinase inhibitor p27 (Kip1) through interacting with the Jun activation domain-binding protein 1 (JAB1) to promote the proliferation of HCC cells [75]."
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"Further research, including clinical based and high-throughput analyses using disease samples and various tumor cell lines, has provided compelling support that CSN5 promotes proliferation."
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"Our results showed that knockdown of CSN5 could inhibit proliferation and promote apoptosis of gastric cancer cells."
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"The key findings of the current study are that BRSK1 down-expression was significantly associated with progression of human breast cancer and that ectopic expression of BRSK1 was inversely regulated b[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"
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"These results demonstrated that Jab1 knockdown inhibited the cellular proliferation of MDA-MB-231 cells which may associate with the specific inhibitory effect on BRSK1 expression."
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"Additionally, using CCK-8 assay, we also found that cell proliferation rate of MDA-MB-231 cells treated with Jab1 siRNA exhibited a significant decrease compared with the negative control siRNA or moc[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"
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"Loss of CSN5 ortholog in D. discoideum , csn5 , severely impairs cell proliferation , suggesting that de-neddylation is important during growth [ 32 ] ."
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"Jab1 promotes glioma cell proliferation by regulating Siah1 and beta-catenin pathway."
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"Thus, Jab1 overexpression contributes to pancreatic cancer cell proliferation and survival."
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"In the current study, we have shown that overexpression of Jab1 stimulated the proliferation of GBC cells; whereas downregulation of Jab1 by using Jab1-siRNA approach resulted in the cell growth inhibition and apoptotic induction."
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"Taken together, our results suggest that HER-2 and neu transcriptionally activates Jab1 expression to promote proliferation of breast cancer cells."
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"A previous study demonstrated that the specific knockdown of COPS5 inhibits the proliferation of colorectal cancer cells, and that COPS5-transgenic mice developed a phenotype similar to that of myeloproliferative disorders."
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"Loss of CSN5 ortholog in D. discoideum , csn5 , severely impairs cell proliferation , suggesting that the cycling of neddylation and de-neddylation is important during growth [ 32 ] ."
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"In line with our previous data, CSN5 knockdown reduced SW480 cell proliferation, whereas it was slightly elevated in DKK1 -depleted cells."
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"Our results show that Stat3 and LAP2 (C/EBP-beta 2) are the two major transcription factors that contribute to Jab1 overexpression that leads to increased proliferation of breast cancer cells."
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"Jab1 may lead to cell proliferation and regulate the cell cycle; it also interacts with p53 inducing phosphorylation mediated by CSN and subsequent degradation."
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"Also, Jab1 activate the c-jun gene resulted cell proliferation."
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"Interestingly, Jab1 appears to induce proliferation, as demonstrated in transfection studies using Jab1 overexpressing HCC cell lines and in siRNA experiments blocking Jab1 expression [2]."
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"It suggests that strong expression of Jab1 not only represents a prognostic marker for malignant transformation but also contributes to cancer cell proliferation and survival."
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"C-Jun activation domain-binding protein-1 ( Jab1 ) , which was initially identified as a c-Jun coactivator , is known to modulate cell proliferation , cell cycle , and apoptosis ."
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"Jab1 promotes cell proliferation and inactivates P27 by inducing translocation of P27 from the nucleus to the cytoplasm , which accelerates P27 degradation through the Ub-dependent proteasome pathway and promotes cell cycle progression [ 34 ] ."
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"This data complements previous studies demonstrating that CSN5 loss inhibits proliferation and induces apoptosis [XREF_BIBR - XREF_BIBR]."
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"As hypothesized, CSN5 and DKK1 double knockdown abrogated the CSN5 knockdown effect, suggesting that DKK1 is involved in CSN5 mediated proliferation effects.To further confirm that secreted supernatan[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"
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"In various human cancer cell lines, the knockdown of CSN5 and JAB1 inhibited the proliferation of tumor cells, suggesting that over-expression of CSN5 and JAB1 not only serves as a marker of malignant transformation, but also actually contributes to tumorigenesis 13."
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"Previous studies have shown that CSN3 and CSN5 could accelerate the cancer cell proliferation and growth XREF_BIBR, XREF_BIBR."
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"Additionally, we found there was a positive correlation between CSN5 and angiopoietin like protein 2 (ANGPTL2) protein levels in thyroid carcinoma tissues and that CSN5 promoted thyroid carcinoma cell proliferation and metastasis through ANGPTL2."
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"These results suggest that overexpression of CSN5 may contribute to both cell survival and proliferation and thus represent a prognostic marker for malignant conversion in liver cancer."
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"Stable form of JAB1 enhances proliferation and maintenance of hematopoietic progenitors."
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"Jab1 and CSN5 knockdown also impaired proliferation and enhanced apoptosis in these cells regardless of the genotype of the tumor suppressor p53 [XREF_BIBR]."
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"Knockdown of CSN5 inhibits the proliferation of human tumor cells XREF_BIBR XREF_BIBR, suggesting that overexpression of CSN5 not only serves as a marker of malignant transformation, but also actually contributes to tumor cell proliferation."
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"The binding of MIF with JAB1 / CSN5 also modulates AP-1 activity and cell proliferation by inactivation of p53 [ 8] ."
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"This interaction suggests that pJAB1 can contribute to the cell proliferation."
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"Second, in a manner independent of the CSN holocomplex, CSN5 (or a CSN5 containing small complex) promotes cell proliferation by inducing p27 degradation [22,23] and HIF1-alpha stabilization [41]."
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"Suppression of Jab1 expression inhibits proliferation and promotes apoptosis of AMC-HN-8 cells."
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"Jab1 and COPS5 knockdown significantly inhibits proliferation and induces apoptosis in hepatocellular carcinoma cells."
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"Cops5 KO leads to decreased expression of the pluripotency marker Nanog, proliferation defect, G2/M cell-cycle arrest, and apoptosis of ESCs."
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"Inhibition of Jab1 not only blocks cancer cell proliferation, but also reduces the DNA HR repair function after cancer therapy."
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"COPS5 inhibition arrests the proliferation and growth of serous ovarian cancer cells via the elevation of p27 level."
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"Jab1 is upstream of p14ARF and promote gastric cancer cell proliferation in vitro and in vivo."
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"Jab1 Silencing Inhibits Proliferation and Sensitizes to Cisplatin in Biliary Tract Cancer."
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"In addition, a high level of Jab1 is observed in a variety of human cancers and is sometimes correlated with a poor prognosis, suggesting that Jab1 contributes to cancer cell proliferation and survival and could be a novel target of cancer therapy."
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